xe991  (Alomone Labs)


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    Structured Review

    Alomone Labs xe991
    K v 7 inhibitor <t>XE991</t> triggers bilateral seizure/spreading depolarization complex and death in K v 1.1 KO mice. After baseline recordings, K v 1.1 KO ( n = 5) and wild-type (WT, n = 4) mice were administered a single dose of XE991 (5–10 mg/kg i.p.), triggering bilateral seizure-spreading depolarization complexes in all K v 1.1 KO mice. ( A ) 60% (3/5) of KO mice acutely survived the seizure-spreading depolarization complex but subsequently died. ( B ) Remaining mice (2/5) died immediately following the bilateral seizure-spreading depolarization. No seizure or spreading depolarization (SD) were detected in four K v 1.1 wild-type control mice and all survived.
    Xe991, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/xe991/product/Alomone Labs
    Average 95 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    xe991 - by Bioz Stars, 2022-11
    95/100 stars

    Images

    1) Product Images from "Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization"

    Article Title: Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization

    Journal: Brain

    doi: 10.1093/brain/awab141

    K v 7 inhibitor XE991 triggers bilateral seizure/spreading depolarization complex and death in K v 1.1 KO mice. After baseline recordings, K v 1.1 KO ( n = 5) and wild-type (WT, n = 4) mice were administered a single dose of XE991 (5–10 mg/kg i.p.), triggering bilateral seizure-spreading depolarization complexes in all K v 1.1 KO mice. ( A ) 60% (3/5) of KO mice acutely survived the seizure-spreading depolarization complex but subsequently died. ( B ) Remaining mice (2/5) died immediately following the bilateral seizure-spreading depolarization. No seizure or spreading depolarization (SD) were detected in four K v 1.1 wild-type control mice and all survived.
    Figure Legend Snippet: K v 7 inhibitor XE991 triggers bilateral seizure/spreading depolarization complex and death in K v 1.1 KO mice. After baseline recordings, K v 1.1 KO ( n = 5) and wild-type (WT, n = 4) mice were administered a single dose of XE991 (5–10 mg/kg i.p.), triggering bilateral seizure-spreading depolarization complexes in all K v 1.1 KO mice. ( A ) 60% (3/5) of KO mice acutely survived the seizure-spreading depolarization complex but subsequently died. ( B ) Remaining mice (2/5) died immediately following the bilateral seizure-spreading depolarization. No seizure or spreading depolarization (SD) were detected in four K v 1.1 wild-type control mice and all survived.

    Techniques Used: Mouse Assay

    Acute enhancement/inhibition of spreading depolarization in wild-type cortex by K v 7 inhibitor/activator in vitro . ( A and B ) Effect of XE991 on spreading depolarization propagation rate and K + threshold. ( A ) Spreading depolarization propagation rate measured from spreading depolarizations repetitively generated in single slices while incubated in the drug was unchanged. Control: 2.4 ± 0.2 mm/min, XE991: 2.8 ± 0.5 mm/min, Wash: 2.6 ± 0.6 mm/min, n = 6, P = 0.37. n.s. = not significant. ( B ) Spreading depolarization threshold was decreased by Kcnq inhibitor in K + bath application model. Control: 11.0 ± 0.2 mM, XE991: 10.0 ± 0.2 mM, n = 12 each, * P
    Figure Legend Snippet: Acute enhancement/inhibition of spreading depolarization in wild-type cortex by K v 7 inhibitor/activator in vitro . ( A and B ) Effect of XE991 on spreading depolarization propagation rate and K + threshold. ( A ) Spreading depolarization propagation rate measured from spreading depolarizations repetitively generated in single slices while incubated in the drug was unchanged. Control: 2.4 ± 0.2 mm/min, XE991: 2.8 ± 0.5 mm/min, Wash: 2.6 ± 0.6 mm/min, n = 6, P = 0.37. n.s. = not significant. ( B ) Spreading depolarization threshold was decreased by Kcnq inhibitor in K + bath application model. Control: 11.0 ± 0.2 mM, XE991: 10.0 ± 0.2 mM, n = 12 each, * P

    Techniques Used: Inhibition, In Vitro, Generated, Incubation

    2) Product Images from "Kcnq2/Kv7.2 controls the threshold and bihemispheric symmetry of cortical spreading depolarization"

    Article Title: Kcnq2/Kv7.2 controls the threshold and bihemispheric symmetry of cortical spreading depolarization

    Journal: bioRxiv

    doi: 10.1101/2020.11.27.401570

    Kv7 inhibitor XE991 triggers bilateral seizure/SD complex and death in Kv1.1 KO mice. After baseline recordings, Kv1.1 KO (n=5) and WT (n=4) mice were administered a single dose of XE991 (5-10 mg/kg i.p.), triggering a bilateral seizure-SD complexes in all Kv1.1 KO mice. A . 60% (3/5) of KO mice acutely survived the seizure-SD complex but subsequently died. B . Remaining mice (2/5 mice) died immediately following the bilateral seizure-SD. No seizure or SD were detected in 4 Kv1.1 WT control mice and all survived.
    Figure Legend Snippet: Kv7 inhibitor XE991 triggers bilateral seizure/SD complex and death in Kv1.1 KO mice. After baseline recordings, Kv1.1 KO (n=5) and WT (n=4) mice were administered a single dose of XE991 (5-10 mg/kg i.p.), triggering a bilateral seizure-SD complexes in all Kv1.1 KO mice. A . 60% (3/5) of KO mice acutely survived the seizure-SD complex but subsequently died. B . Remaining mice (2/5 mice) died immediately following the bilateral seizure-SD. No seizure or SD were detected in 4 Kv1.1 WT control mice and all survived.

    Techniques Used: Mouse Assay

    Acute Enhancement/Inhibition of SD in WT cortex by Kv7 inhibitor/activator in vitro. A B . Effect of XE991 on SD propagation rate and K + threshold. A . SD propagation rate measured from SD repetitively generated in single slices while incubated in the drug was unchanged. n.s = not significant, n=6. B . SD threshold was decreased by Kcnq inhibitor in K + bath application model. n=12 each * p
    Figure Legend Snippet: Acute Enhancement/Inhibition of SD in WT cortex by Kv7 inhibitor/activator in vitro. A B . Effect of XE991 on SD propagation rate and K + threshold. A . SD propagation rate measured from SD repetitively generated in single slices while incubated in the drug was unchanged. n.s = not significant, n=6. B . SD threshold was decreased by Kcnq inhibitor in K + bath application model. n=12 each * p

    Techniques Used: Inhibition, In Vitro, Generated, Incubation

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    Alomone Labs xe991
    Potassium channels regulate the cellular internalization of various TAT-bound cargos. ( A ) TAT-PNA-induced luciferase activity in the indicated cell lines pretreated or not with potassium channel inhibitors <t>(XE-991</t> or TRAM-34) or genetically invalidated for specific potassium channels. Results are normalized to non-stimulated cells (dashed lines). The independent experiment replicates are color-coded. The p-values correspond to the assessment of the significance of the differences with the control wild-type (WT) condition using ANOVA multiple comparison analysis with Dunnett’s correction. ( B ) Representative microscopy images of WT and KCNQ5 knock-out (KO) Raji cells expressing loxP-RFP-STOP-loxP-GFP and treated or not with 20 μM TAT-Cre for 48 hr. The results correspond to one of three independent experiments. ( C ) Internalization, recorded by flow cytometry, of FITC-D-JNKI1 after 1 hr of incubation in the indicated cell lines genetically invalidated (KO) or not (WT) for specific potassium channels. The results correspond to the median of three independent experiments.
    Xe991, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/xe991/product/Alomone Labs
    Average 95 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    xe991 - by Bioz Stars, 2022-11
    95/100 stars
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    Image Search Results


    Potassium channels regulate the cellular internalization of various TAT-bound cargos. ( A ) TAT-PNA-induced luciferase activity in the indicated cell lines pretreated or not with potassium channel inhibitors (XE-991 or TRAM-34) or genetically invalidated for specific potassium channels. Results are normalized to non-stimulated cells (dashed lines). The independent experiment replicates are color-coded. The p-values correspond to the assessment of the significance of the differences with the control wild-type (WT) condition using ANOVA multiple comparison analysis with Dunnett’s correction. ( B ) Representative microscopy images of WT and KCNQ5 knock-out (KO) Raji cells expressing loxP-RFP-STOP-loxP-GFP and treated or not with 20 μM TAT-Cre for 48 hr. The results correspond to one of three independent experiments. ( C ) Internalization, recorded by flow cytometry, of FITC-D-JNKI1 after 1 hr of incubation in the indicated cell lines genetically invalidated (KO) or not (WT) for specific potassium channels. The results correspond to the median of three independent experiments.

    Journal: eLife

    Article Title: Genetic, cellular, and structural characterization of the membrane potential-dependent cell-penetrating peptide translocation pore

    doi: 10.7554/eLife.69832

    Figure Lengend Snippet: Potassium channels regulate the cellular internalization of various TAT-bound cargos. ( A ) TAT-PNA-induced luciferase activity in the indicated cell lines pretreated or not with potassium channel inhibitors (XE-991 or TRAM-34) or genetically invalidated for specific potassium channels. Results are normalized to non-stimulated cells (dashed lines). The independent experiment replicates are color-coded. The p-values correspond to the assessment of the significance of the differences with the control wild-type (WT) condition using ANOVA multiple comparison analysis with Dunnett’s correction. ( B ) Representative microscopy images of WT and KCNQ5 knock-out (KO) Raji cells expressing loxP-RFP-STOP-loxP-GFP and treated or not with 20 μM TAT-Cre for 48 hr. The results correspond to one of three independent experiments. ( C ) Internalization, recorded by flow cytometry, of FITC-D-JNKI1 after 1 hr of incubation in the indicated cell lines genetically invalidated (KO) or not (WT) for specific potassium channels. The results correspond to the median of three independent experiments.

    Article Snippet: XE-991 and TRAM-34 (Alomone Labs, ref no. X-100 and T-105, respectively) was dissolved in DMSO at 100 mM and stored at –20°C.

    Techniques: Luciferase, Activity Assay, Microscopy, Knock-Out, Expressing, Flow Cytometry, Incubation

    Potassium channels modulate direct cell-penetrating peptide (CPP) translocation, but not endocytosis. ( A ) Same as Figure 2C , but for wild-type (WT), KCNN4 and KCNK5 SKW6.4 knock-out (KO) cells. The results correspond to the average of three independent experiments. ( B ) As panel A, but for WT and KCNN4 KO HeLa cells. The results correspond to the average of three independent experiments. ( C ) Quantitation by flow cytometry of 20 μg/ml AlexaFluor488-transferrin (left) or 200 μg/ml 10 kDa FITC-Dextran (right) internalization in the indicated WT cell lines and their corresponding KO versions, pretreated or not for 30 min with the XE-991 (10 μM) or TRAM-34 (10 μM) potassium channel inhibitors. Transferrin and dextran internalization was allowed to proceed for 60 min (still in the presence of inhibitors when these were used in the 30 min pre-incubation period). To quench membrane-bound fluorescence, cells were incubated with 0.2% trypan blue prior to flow cytometry analysis. The independent experiment replicates are color-coded. ( D ) Assessment of FITC-TAT-RasGAP 317-326 cell surface binding on WT and KCNQ5 KO Raji cells after 60 s of incubation (top), as well as associated peptide internalization after 1 hr of treatment (bottom). The results correspond to at least five independent experiments.

    Journal: eLife

    Article Title: Genetic, cellular, and structural characterization of the membrane potential-dependent cell-penetrating peptide translocation pore

    doi: 10.7554/eLife.69832

    Figure Lengend Snippet: Potassium channels modulate direct cell-penetrating peptide (CPP) translocation, but not endocytosis. ( A ) Same as Figure 2C , but for wild-type (WT), KCNN4 and KCNK5 SKW6.4 knock-out (KO) cells. The results correspond to the average of three independent experiments. ( B ) As panel A, but for WT and KCNN4 KO HeLa cells. The results correspond to the average of three independent experiments. ( C ) Quantitation by flow cytometry of 20 μg/ml AlexaFluor488-transferrin (left) or 200 μg/ml 10 kDa FITC-Dextran (right) internalization in the indicated WT cell lines and their corresponding KO versions, pretreated or not for 30 min with the XE-991 (10 μM) or TRAM-34 (10 μM) potassium channel inhibitors. Transferrin and dextran internalization was allowed to proceed for 60 min (still in the presence of inhibitors when these were used in the 30 min pre-incubation period). To quench membrane-bound fluorescence, cells were incubated with 0.2% trypan blue prior to flow cytometry analysis. The independent experiment replicates are color-coded. ( D ) Assessment of FITC-TAT-RasGAP 317-326 cell surface binding on WT and KCNQ5 KO Raji cells after 60 s of incubation (top), as well as associated peptide internalization after 1 hr of treatment (bottom). The results correspond to at least five independent experiments.

    Article Snippet: XE-991 and TRAM-34 (Alomone Labs, ref no. X-100 and T-105, respectively) was dissolved in DMSO at 100 mM and stored at –20°C.

    Techniques: Translocation Assay, Knock-Out, Quantitation Assay, Flow Cytometry, Incubation, Fluorescence, Binding Assay